When doctors won't tell . . .
Of all the online nutritional information, nutritional facts, medical and
dietary sites there are to choose from, in an article entitled "How
to ease the pain" The Sunday Times magazine,
Culture, published a list of just five websites it
considered reliable and informative.This site was one of that five.

CONDITIONS
AND DISEASES PREVENTED AND HELPED BY A LOW-CARB, HIGH-FAT DIET

SOY & DES (Diethylstilbestrol)

Diethylstilbestrol
is a synthetic estrogen that caused cancerous birth defects in the
daughters of women who took it while pregnant. The defects did not
become apparent until those young women reached maturity. Subsequent
events showed that male reproductive function was also impaired.
DES is so potent and harmful that it is banned as a residue of growth
promoters in beef liver at one part in two billion. The UK Food
Surveillance program knew that a Government laboratory, the Central
Veterinary laboratory, had established by 1980 that soy food for
human consumption had an estrogenic equivalence of more than 16
parts per billion of DES. The abstract of that work by Drane
et al is posted at the foot of this page. Also posted here are
numerous warnings by other scientists of the equivalent danger from
soy foods.

Soy Information Service believes
that regulators all over the world have ignored these warnings for
political reasons; the "Precautionary Principle" dictated
that that consumers be protected from these hazards by decrees that
isoflavones be removed from soy products for human consumption.
That they did not do so may be behind the alarming increase in
UK birth defects and hormonal cancers
and to the decrease in sperm quality
and quantity. Further evidence that exposure of a pregnant
woman to estrogenic toxins can be devastating for her child in later
life can be found Here.

Where's the Proof? Read on.

Follow this link to an Endocrine
Disruptors and Man-made Chemicals Timeline which provides information,
historical use and discovery of the harmful effects chemicals like
DES can have on people. Research as far back as 1952 showed
"...that DES actually increases the number of miscarriages,
premature births, and deaths among infants".

What to have for Breakfast?

A slice of "sheila bread" (Burgen's Soy and Linseed)
is at the cancer-risk level that caused diethylstilbestrol to be
banned from meat as a growth promoter'.

"Estrogenic
Activity of Burgen Bread to Female Rats"

Ashby J., and Tinwell H.

Journal of Human and Experimental Toxicology (1998) (17) pp 394-399.

In this research a four day dose of soy & linseed bread caused
the uterus weights of female rats to DOUBLE . AND one slice (34
gr) of Burgen bread had estrogenic equivalence of 0.5 ppb of Diethylstilbestrol

Quotes

There is concern that environmental exposure of humans to synthetic
oestrogens may be responsible for the reported declines in human
sperm quality and increases in the incidence of human reproductive
organ cancers. This has led to extensive international efforts to
devise/refine assays for the identification of synthetic oestrogens
such as diethylstilboestrol (DES) and nonylphenol (NP) and to institute
appropriate regulatory measures to control their release into the
environment. A major complication to these endeavours is the extensive
dietary exposure of humans to plant oestrogens (phytoestrogens),
the potential hazards/benefits of which remain uncertain.

Burgen brown bread was recently introduced into the United Kingdom
with the implication that it can ease post-menopausal symptoms in
women. It is enriched with an unspecified quantity of soya flour
and linseed, both of which contain phytoestrogens. The advertisements
and the wrapper state that Burgen bread is high in natural plant
oestrogens and a variety of anecdotal endorsements are offered including
that it is capable of putting the ‘waltz back into Matilda'. The
telephone help-line provided adds to the clinical area of the product.
We report here the estrogenic activity of Burgen bread in the immature
rat uterotrophic assay, one of the most well established methods
of assessing the estrogenic potential of chemicals. The test relies
on the ability of oestrogens such as DES and NP to induce precocious
growth of the uterus of sexually immature (weanling) animals and
provides information on the potential hormonal activity of chemicals
to estrogen-responsive tissues of humans.

Access of weanling female AP rats to Burgen bread as their sole
food for 4 days led to a doubling or uterus weights on the fifth
day. The positive control agent DES (in arachis oil (AO)) increased
uterus weights fourfold in that encountered in sexually mature young
rats. Normal laboratory rat diet (RMI). AO, and similar access to
Hovis brown bread, were without activity in the assay. The synthetic
environmental oestrogen NP (as its maximum activity close level
in AO) gave a uterotrophic response of similar magnitude in that
given by Burgen bread. Comparison of these data indicates that one
slice of Burgen bread (~34 g) is of equal oestrogenic activity to
the rat uterus as the daily administration of ~0.5 m g of the hormonal
drug DES or 30 mg of the industrial chemical NP.

Organisation versus Activation:
The Role of Endocrine-disrupting Contaminants (EDCs) during Embryonic
Development in Wildlife.

Guillette L. J. Jr, Crain
D. A., Rooney A. A., Pickford D. B.

Environmental Health Perspectives
103 (7) 1995, 157-164.

Abstract

Many environmental contaminants
disrupt the vertebrate endocrine system. Although they may
be no more sensitive to endocrine-disrupting contaminants (EDCs)
than other vertebrates, reptiles are good sentinels of exposure
to EDCs due to the lability in their sex determination. This
is exemplified by a study of alligators at Lake Apopka, Florida,
showing that EDCs have altered the balance of reproductive hormones
resulting in reproductive dysfunction. Such alterations may
be activationally or organizationally induced. Much research
emphasizes the former, but a complete understanding of the influence
of EDCs in nature can be generated only after consideration of both
activational and organizational alterations. THe organizational
model suggests that a small quantity of an EDC, administered during
a specific period of embryonic development, can permanently modify
the organization of the reproductive, immune, and nervous systems.
Additionally, this model helps explain evolutionary adaptations
to naturally occurring estrogenic compounds, such as phytoestrogens.

Quotes

In rodents, exposure to estrogenic
compounds during in utero development or immediately after birth
results in pathological changes of the reporductive tract, as well
as functional differences at puberty and throughout adulthood.
Similar estrogenic effects have also been demonstrated on the immune
and neuroendocrine systems.

Many of the observed DES-induced
modifications to the reproductive system are morphologically subtle
but result in major functional changes.

Although changes in receptor
type and abundance can be considered subtle, developmental abnormalities
of this type may be the basis for infertility or reproductive cancers.

The mechanisms of action
of estrogens on the immune system appear to involve both lymphoid
and nonlymphoid tissues. Estrogen receptors are present at
low levels in lymphoid cells and near uterine levels in thymic epithelium.
EDCs may alter estrogen receptor levels in immune tissues, similar
to receptor changes of the reprodutive system.

A complication when examining
the immune or reproductive systems is the interwoven nature of their
function.

Endocrine irregularities
associated with this T-lymphocyte deficiency include delays in puberty
in females, alterations in normal adenohypophysis formation, and
abnormal circulating levels of gonadal hormones.

Interestingly, it is also
important to note that many organizational modifications do not
become apparent until later in life.

"While the
potency of DES far exceeds that of either the endogenous estrogens,
or the phytoestrogens, the amounts of the latter consumed are significantly
greater. The effects of plant estrogens in man should be of some
concern, since it has been suggested that soya might be as beneficial
as a growth promoter as DES is in animals. For example, the concentrations
of phytoestrogens insoy (calculated to match 0.5 ppb of DES) are
well within the concentration range of consumed soya products"

The developing fetus is uniquely
sensitive to perturbation withestrogenic chemicals.
The carcinogenic effect of prenatal exposureto diethylstilbestrol
(DES) is the classic example. Becausephytoestrogen use
in nutritional and pharmaceutical applicationsfor infants
and children is increasing, we investigated thecarcinogenic
potential of genistein, a naturally occurring plantestrogen
in soy, in an experimental animal model previouslyreported
to result in a high incidence of uterine adenocarcinomaafter
neonatal DES exposure. Outbred female CD-1 mice were treatedon days 1–5 with equivalent estrogenic doses of DES (0.001mg/kg/day) or genistein (50 mg/kg/day). At 18 months, the
incidenceof uterine adenocarcinoma was 35% for genistein
and 31% forDES. These data suggest that genistein is
carcinogenic if exposureoccurs during critical periods
of differentiation. Thus, theuse of soy-based infant
formulas in the absence of medical necessityand the
marketing of soy products designed to appeal to childrenshould
be closely examined.

"Despite
concerns over the deleterious effects of diethylstilbestrol...it
is apparent that the contribution of plant estrogens is rarely considered.This is surprising since the levels of phytoestrogens
in foods is substantially higher than the estrogen levels in animal
tissues.....Our observations in cheetahs further support
serious consideration of the potential implications of dietary estrogens
in humans"

"The Case for Expanded
Phytoestrogen Research"

Sheehan, D.M.

P.S.E.B.M. 1992, 208
pp 3-5.

"Phytoestrogens
have some of the same capabilities to induce developmental toxicity
as do other estrogens... given the DES tragedy, it would be foolish
to ignore the possibility that phytoestrgens constitute
a developmental hazard"

"it
is likely that the genotoxicity of the estrogens acts in concert
with their hormonal activity to give rise to their carcinogenic
effects....it has long been known that estrogenic activity is not
limited to steroidal hormones. In 1938, the stilbene estrogen
diethylstilbestrol was synthesised and found to match or even exceed
E2 in therms of hormonal activity."

"Daughters
born to mothers who took DES now suffer increased rates of clear-cell
cancer, various genital tract abnormalities, abnormal pregnancies
and some changes in immume response. Both sons and daughters
experience congenital abnormalities of their reproductive systemand
reduced fertility".

Isoflavone content of soya-based laboratory
animal diets.

Murphy PA, Farmakalidis E, Johnson LD

Food Chem Toxicol 1982 Jun 20:3 315-7

Quotes:

"The soy phytoestrogens have a number
of pharmocological activities, including the ability to promote
tumor growth...just as the naturally occurring mammalian estrogens
do."

" The concentrations of soy phytoestrogens,
calculated to match 0.5ppb DES, are well within the concentration
range of most soy products examined".

"Mice were followed to evaluate
the potential risk for histological abnormalities, including uterine
tumors later in life. Many of the long-term effects observed after
DES treatment, including uterine adenocarcinoma, were observed after
development exposure to genistein."

Excerpts from the report "The
Toxicity of Soybeans and Related Products"

Allan Aspell and Associates:
Scientific Consultants

Author M. G. Fitzpatrick PhD
March 31 1994.

DES is a synthetic, non-steroidal
estrogen which was used as a growth stimulant in cattle and sheep.
DES daughters, born to mothers who used DES during pregnancy, have
a much higher probability of cervicovaginal abnormalities, such
as incomplete cervical collar and vaginal adenosis (a condition
characterised by the presence of non-malignant glandular tissue
in the vagina) (Kincl, 1990). Ultimately, this has had an
effect on the fertility of DES daughters. Women with gross
cervical abnormalities have a threefold increase in the incidence
of miscarriage compared with other women. DES daughters also
have greater difficulty conceiving than their peers (Apfel and Fisher,
1984). There is also a strong association between clear cell
adenocarcinoma, a rare form of malignant vaginal cancer, and fetal
exposure to DES (Apfel and Fisher, 1984). DES sons were also
affected; the incidence of genitourinary abnormalities and infertility
is higher in exposed males (Kincl, 1990). Follow up studies
on physical changes in DES sons have not received detailed attention;
such studies are difficult since there is no single condition, such
as adenosis in the female, that typifies exposure to DES (Apfel
and Fisher, 1984).

The significant effects of DES on
the fetus, and that DES syndrome can also be caused by other exogenous
estrogens (Amdur et al 1993) has stigmatised the use of estrogens
in humans (Kirk et al 1978); modern medical practice is to avoid
their use during pregnancy (Apfel and Fisher, 1984).

Fetal cells are generally less sensitive
to endogenous estrogens than those of the mother; exceptions are
tissues of the vagina, uterus and breast of female fetuses, and
the prostate tissue of male fetuses (Apfel and Fisher, 1984).
The fetus may be especially sensitive to exogenous estrogens; this
is the case with DES. DES exposure probably sensitised the
fetus to all estrogens, hence, increasing the vulnerability to the
carcinogenic effects of estrogens later on in life (Apfel and fisher
1984). DES cancer may develop 20 years to 25 years after transplacental
exposure, highlighting the often delayed effects that prenatal exposure
to estrogens can have.

From "Cellular and Mollecular
Mechanisms of Hormonal Carcinogenisis..Environmental Influences"

ISBN 0-471-02202-0

Chapter 6 'Mechanisms of Estrogen-Associated
Carcinogenesis'

by Dr J.Carl

Bennett and Dr Takeki Tsutsui

Of US NIEHS at Research Triangle
Park, NC 27709; and the Dept ofPharmocology, Nippon School of Dentistry,
Tokyo 102, Japan.

" There is stong evidence from
several systems to support the hypothesis that estrogens are epigenic
carcinogens, acting via a promoting effect related to stimulation
of proliferation of estrogen-responsive cells..........Tumors are
induced by both D E S and 17B estradiol.....both induce transformation
of hamster cells that is indistinguishable from that induced by
other chemical carcinogens...sarcomas are also induced by subcutaneous
injection of Syrian hamsters."

Normal
rat cake containing soya meal was found to be oestrogenic.
Sixteen samples of soya meal were examined in the mouse uterine
bioassay and all were found to have oestrogenic activity.
Ethyl-acetate extracts of the meals also had oestrogenic activity.
Genistein and daidzein were present in the extracts.

Excerpts

Little
attention seems to have been paid to soya meal as a possible source
of oestrogenicity although daidzein and genistein were isolated
from soya beans nearly 50 years ago (Walz, 1931).

Various
reproductive disturbances in animals have been traced to the ingestion
of oestrogenic feeds.

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